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A7045 - Acute Reversible Pulmonary Hypertension: A Rare and Dangerous Complication of Cocaine Use
Author Block: T. Kukkadapu1, T. Singh1, J. Keshavamurthy2, S. Taylor2, G. Sharma3; 1Augusta University, Augusta, GA, United States, 2Radiology, Augusta University, Augusta, GA, United States, 3Cardiology, Augusta University, Augusta, GA, United States.
Introduction:
Cocaine is known to cause chronic pulmonary hypertension, but there have been rare reports of acute reversible pulmonary hypertension attributed to cocaine use. We present a case of acute right heart failure caused by cocaine induced pulmonary hypertension.
Case:
37 year old African American female presented with chest pain after using cocaine. Physical exam was remarkable for cold extremities and tachycardia. She was hemodynamically unstable at presentation with blood pressure of 60/40 mmHg and heart rate of 134 beats per minute. Electrocardiogram showed ST elevations in V2-V4 leads and ST depressions in leads II, III and aVF. Troponins were 29.8; patient was started on norepinehrine drip and immediately taken to catheterization lab. Left heart catheterization revealed normal coronaries and normal left ventricular ejection fraction. Right heart catheterization showed elevated pulmonary artery (PA) pressures at 25 mmHg, right ventricular (RV) pressures at 24 mmHg and normal pulmonary capillary wedge pressures (PCWP) at 15 mmHg. Transthoracic echocardiogram exhibited severely dilated RV and severely reduced RV function. CT angiogram (CTA) chest showed no pulmonary embolism, but demonstrated increased RV/LV ratio and reflux of contrast material into the inferior vena cava and hepatic veins. Findings were consistent with cardiogenic shock due to RV failure, likely secondary to acute pulmonary hypertension from cocaine use. Patient was transferred to a tertiary care center for further management. Patient is still alive a year later.
Discussion:
Chronic pulmonary hypertension is associated with cocaine use; it is thought to be multifactorial resulting from foreign particle inhalation causing chronic granulomatous disease and fibrosis, micro thromboembolic disease and chronic morphologic alterations in pulmonary artery. However, none of these mechanisms explain cocaine induced acute pulmonary hypertension. Cocaine-induced arteriolar vasoconstriction is well known; however, its effects on pulmonary vasculature have not been well studied. As 20% of cocaine users were found to have medial hypertrophy of pulmonary vasculature on autopsy, it can be postulated that transient vasospasm with each cocaine use can lead to smooth muscle proliferation over time. Endothelin-1, a known vasoconstrictor, has also been isolated from bronchoalveolar lavage samples of cocaine users. A study by Kleerup et al failed to show any rise in PA pressures with intranasal cocaine administration; however, it was limited by a small sample size of 10 subjects. Our case accentuates the need for further larger studies to look into mechanisms by which cocaine can induce acute pulmonary hypertension.